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Related Concept Videos

GPCRs Regulate Adenylyl Cylase Activity01:09

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G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
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Heterotrimeric G proteins are guanine nucleotide-binding proteins. As the name suggests, heterotrimeric G proteins are composed of three subunits: alpha, beta, and gamma. They remain GDP-bound or GTP-bound inside the cells and switch between inactive/active states. The Gα subunit possesses the nucleotide-binding pocket that binds guanine nucleotides and switches between GDP or GTP-bound states. In contrast, the Gꞵ and Gγ subunits are always bound together with high...
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β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
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Total ginsenosides decrease Aβ production through activating PPARγ.

Shan He1, Junhe Shi2, Lina Ma2

  • 1Wangjing Hospital, China Academy of Chinese Medical Sciences, Beijing, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|April 9, 2024
PubMed
Summary
This summary is machine-generated.

Total ginsenosides (TG) from ginseng improve memory and reduce amyloid-beta (Aβ) in Alzheimer

Keywords:
Alzheimer’s diseaseAmyloid βBACE1NF-κBPPARγ

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is a neurodegenerative disorder characterized by amyloid-beta (Aβ) plaque accumulation.
  • Total ginsenosides (TG), derived from ginseng, show potential therapeutic benefits for AD.
  • The precise mechanism by which TG exerts its effects in AD remains largely undetermined.

Purpose of the Study:

  • To elucidate the underlying mechanism of Total Ginsenosides (TG) in ameliorating Alzheimer's disease (AD) pathology.
  • To investigate the role of PPARγ in mediating the effects of TG on amyloid-beta (Aβ) production and cognitive function.

Main Methods:

  • Utilized APP/PS1 transgenic mice and N2a/APP695 cells as in vivo and in vitro models, respectively.
  • Assessed cognitive function using the Morris water maze (MWM) and neuronal changes via H&E and Nissl staining.
  • Quantified Aβ deposition, gene/protein expression (BACE1, PS1, PS2), and NF-κB p65 translocation, employing immunofluorescence, Western blotting, and qRT-PCR.

Main Results:

  • TG treatment significantly improved spatial learning and memory in APP/PS1 mice.
  • TG administration reduced Aβ accumulation in the cortex and hippocampus of mice.
  • TG acted as a PPARγ agonist in cells, inhibiting NF-κB p65 translocation and decreasing Aβ1-40/Aβ1-42 secretion and amyloidogenic gene expression.

Conclusions:

  • Total ginsenosides (TG) effectively reduce amyloid-beta (Aβ) production both in vivo and in vitro.
  • Activation of PPARγ by TG is a key mechanism for facilitating Aβ clearance and improving cognitive deficits in an AD mouse model.